The ventromedial portion of the hypothalamus (satiety center) is an essential link in a regulator system which adjusts food intake to energy output ss that the weight of the mature animal remains fairly constant. The critical role of the satiety center in this system is demonstrated by the gross increase in voluntary food intake, and the resultant obesity, which follow ablation of the center. Our broad objectives are to elucidate the physiology of the center and the biochemical properties underlying its function. It may be reasonably anticipated that understanding of the factors which influence satiity center activity will be useful in the management of the clinically important problem of obesity. We have found that the center responds to insulin, glucocorticoids and inhibitors of glucose utilization and that specific glucoreceptor cells are present in the center. Changes in feeding behavior are correlated with changes in the activity of the center produced by these agents. In exploitation of these findings, we wish to explore further the physiological, biochemical and anatomical characteristics underlying the function of this region of the brain in its control of feeding behavior. In the intact mouse, the suscetibility of the satiety center to gold thioglucose-induced necrosis, which can be taken as an index of the functional activity of the center, as well as feeding behavior will be used in assaying the influence of other hormone and metabolites known to affect glucose metabolism.